V
Vanesa Gottifredi
Researcher at Fundación Instituto Leloir
Publications - 62
Citations - 2461
Vanesa Gottifredi is an academic researcher from Fundación Instituto Leloir. The author has contributed to research in topics: DNA replication & DNA damage. The author has an hindex of 26, co-authored 58 publications receiving 2198 citations. Previous affiliations of Vanesa Gottifredi include Columbia University & National Scientific and Technical Research Council.
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p53 Linear Diffusion along DNA Requires Its C Terminus
TL;DR: It is shown here that wild-type p53 possesses the ability to linearly diffuse on DNA, and that the C terminus is a positive regulator of DNA binding in vivo and in vitro, and indicate that the mechanism may involve linear diffusion.
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p53 accumulates but is functionally impaired when DNA synthesis is blocked.
TL;DR: Stalled replication forks activate kinases that modify and stabilize p53, yet act downstream of ATM to impair p53 transcriptional activity, suggesting that blocked DNA replication prevents p53 from being fully active as a transcription factor.
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p53 Down-Regulates CHK1 through p21 and the Retinoblastoma Protein
TL;DR: It is suggested that p53 andCHK1 play interdependent and complementary roles in regulating both the arrest and resumption of G2 after DNA damage and the possible involvement of E2F-dependent transcription in the regulation of CHK1.
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Mitochondrial fusion is essential for steroid biosynthesis.
Alejandra Duarte,Cecilia Poderoso,Mariana Cooke,Gastón Soria,Fabiana Cornejo Maciel,Vanesa Gottifredi,Ernesto J. Podestá +6 more
TL;DR: It is shown that the hormonal stimulation triggers mitochondrial fusion into tubular-shaped structures and it is demonstrated that mitochondrial fusion does not only correlate-with but also is an essential step of steroid production, being both events depend on PKA activity.
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From the Cover: p53 accumulates but is functionally impaired when DNA synthesis is blocked
TL;DR: The ability of cells to induce p53 in response to potentially mutagenic or oncogenic events has a crucial role in preventing malignant progression as discussed by the authors, which is manifested by increased levels and activity of the protein through posttranscriptional mechanisms.